ICAD Cancer Research Results

ICAD, inhibitor of caspase-activated DNase: Click to Expand ⟱
Source:
Type:
ICAD (inhibitor of caspase-activated DNase, also known as DFFA)
ICAD is the physiological inhibitor of CAD, the nuclease responsible for executing DNA fragmentation during apoptosis.
• Caspase-mediated cleavage of ICAD is a key regulatory step that unleashes CAD activity during apoptosis.

Its dysregulation (either up‐ or down‐regulation) has been linked to altered apoptotic responses, genomic instability, and ultimately clinical outcomes.
Either overexpression or underexpression can disrupt this balance:
▪ Overexpression may blunt the full execution of apoptosis in response to stresses (e.g., chemotherapy).
▪ Underexpression may lead to unscheduled or incomplete apoptosis, which in some scenarios might paradoxically fuel genomic instability.
Pca, Prostate Cancer: Click to Expand ⟱
Prostate Cancer: Alterations in genes such as ERG, SPOP, MYC, androgen receptor (AR), and CHD1, drive PCa progression.
TP53 is the most commonly mutated gene in human cancer.
HH↑, GLI-1↑, SHH↑ P53↓
The loss of p53 and/or other tumor suppressor genes, reduced capacity for DNA repair, the dysfunction of telomerase activity, and changes in the pathways that govern the growth of cells also mediate the progression of Pca.
It has been well documented that Ca2+ influx and MDR1 upregulation are highly associated with GEM metabolism in human pancreatic carcinoma.
Increased Growth factor IGF-1/IGF-1R axis activation mediated by both PI3K/Akt or RAF/MEK/ERK system and AR expression remains important in the development and progression of prostate cancer.
It has been demonstrated that prostate cancer cells are relatively sensitive to heat stress.
Long non-coding RNA MALAT1 has been reported as an oncogenic target in multiple types of cancers, including PC.
Scientific Papers found: Click to Expand⟱
3192- SFN,    Transcriptome analysis reveals a dynamic and differential transcriptional response to sulforaphane in normal and prostate cancer cells and suggests a role for Sp1 in chemoprevention
- in-vitro, Pca, PC3
Sp1/3/4↓, selectivity↑, NRF2↑, HDAC↓, DNMTs↓, TumCCA↑, selectivity↑, HO-1↑, NQO1↑, CDK2↓, TumCP↓, BID↑, Smad1↑, Diablo↑, ICAD↑, Cyt‑c↑, IAP1↑, HSP27↑, *Cyt‑c↓, *IAP1↓, *HSP27↓, survivin↓, CDK4↓, VEGF↓, AR↓,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

HO-1↑, 1,   NQO1↑, 1,   NRF2↑, 1,  

Cell Death ⓘ

BID↑, 1,   Cyt‑c↑, 1,   Diablo↑, 1,   IAP1↑, 1,   ICAD↑, 1,   survivin↓, 1,  

Kinase & Signal Transduction ⓘ

Sp1/3/4↓, 1,  

Protein Folding & ER Stress ⓘ

HSP27↑, 1,  

DNA Damage & Repair ⓘ

DNMTs↓, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

HDAC↓, 1,  

Migration ⓘ

Smad1↑, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature ⓘ

VEGF↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

selectivity↑, 2,  

Clinical Biomarkers ⓘ

AR↓, 1,  
Total Targets: 22

Pathway results for Effect on Normal Cells:


Cell Death ⓘ

Cyt‑c↓, 1,   IAP1↓, 1,  

Protein Folding & ER Stress ⓘ

HSP27↓, 1,  
Total Targets: 3

Scientific Paper Hit Count for: ICAD, inhibitor of caspase-activated DNase
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:22  Cells:%  prod#:%  Target#:877  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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